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Interplay between pathway-specific and global regulation of the fumonisin gene cluster in the rice pathogen Fusarium fujikuroi

Rösler, Sarah M., Sieber, Christian M. K., Humpf, Hans-Ulrich, Tudzynski, Bettina
Applied microbiology and biotechnology 2016 v.100 no.13 pp. 5869-5882
Fusarium fujikuroi, Fusarium verticillioides, biosynthesis, corn, fumonisins, fungi, gene overexpression, germplasm conservation, gibberellins, host specificity, multigene family, nitrogen, pathogens, pigments, rice, secondary metabolites, seedlings, seeds, transcription factors
The rice pathogenic fungus Fusarium fujikuroi is known to produce a large variety of secondary metabolites. Besides the gibberellins, causing the bakanae effect in infected rice seedlings, the fungus produces several mycotoxins and pigments. Among the 47 putative secondary metabolite gene clusters identified in the genome of F. fujikuroi, the fumonisin gene cluster (FUM) shows very high homology to the FUM cluster of the main fumonisin producer Fusarium verticillioides, a pathogen of maize. Despite the high level of cluster gene conservation, total fumonisin FB₁ and FB₂ levels (FBₓ) produced by F. fujikuroi were only 1–10 % compared to F. verticillioides under inducing conditions. Nitrogen repression was found to be relevant for wild-type strains of both species. However, addition of germinated maize kernels activated the FBₓ production only in F. verticillioides, reflecting the different host specificity of both wild-type strains. Over-expression of the pathway-specific transcription factor Fum21 in F. fujikuroi strongly activated the FUM cluster genes leading to 1000-fold elevated FBₓ levels. To gain further insights into the nitrogen metabolite repression of FBₓ biosynthesis, we studied the impact of the global nitrogen regulators AreA and AreB and demonstrated that both GATA-type transcription factors are essential for full activation of the FUM gene cluster. Loss of one of them obstructs the pathway-specific transcription factor Fum21 to fully activate expression of FUM cluster genes.